The hypotheses to be tested are as follows: The Gulf War syndrome is due to exposure to combinations of organophosphates in the war that caused brainstem injury. Malfunction of the brainstem regulatory processes are causing central sleep apnea, which is producing sympathetic nerve hyperactivity through peripheral or central chemoreflex sensitization, resulting in a form of neurogenic hypertension. Alternatively, it is possible that injured microglia in the area of brainstem injury are overproducing interleukin-6, which in turn is stimulating overproduction of cortisol, norepinephrine and sympathetic nervous system activity, as has recently been found in patients after CVA's. Pharmacologically interrupting the metabolic consequences of the brainstem dysfunction may provide substantial relief from many of the symptoms of Gulf War syndrome.